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Frontiers in Tropical Diseases ·

Volume 7 - 2026 | https://doi.org/10.3389/fitd.2026.1960706

The global emergence of Trichophyton indotineae: epidemiology, resistance, and management challenges

  • Dipika Shaw1
  • Adnan Omar2
  • Michelle Singh2
  • Merin Chandanathil3
  • Chandana Bhargavi4
  • Nagaraj Mysore5
  • Dharam Bir6
  • Srinidhi Ramasamy2
  • Prasanna Honnavar7*corresponding author
  1. 1Department of Microbiology, Uma Nath Singh Autonomous State Medical College, Jaunpur, Uttar Pradesh, India
  2. 2Basic Medical Science, American University of Antigua College of Medicine, Coolidge, Antigua and Barbuda
  3. 3Department of Physiology, American University of Antigua College of Medicine, Coolidge, Antigua and Barbuda
  4. 4Department of Anatomy and Medical Imaging, American University of Antigua College of Medicine, Coolidge, Antigua and Barbuda
  5. 5Department of Clinical Medicine, American University of Antigua College of Medicine, Coolidge, Antigua and Barbuda
  6. 6Brown Center for Immunotherapy, Melvin and Bren Simon Comprehensive Cancer Center, Division of Hematology and Oncology, School of Medicine, Indiana University, Indianapolis, IN, United States
  7. 7Department of Microbiology and Immunology, American University of Antigua College of Medicine, Coolidge, Antigua and Barbuda
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Abstract

Dermatophytosis affects approximately 25% of the world population. Terbinafine, an antifungal medication, was historically used to treat this condition. However, the infection caused by a newer fungal species called Trichophyton indotineae has changed this situation, as it responds poorly to terbinafine. Moreover, the infection caused by this species lasts longer, returns repeatedly after treatment, and can spread over large areas of the body. This fungus was first linked to major recurrent and chronic skin infections in India and has now spread across the globe having been identified in Asia, the Middle East, Europe, and North America. The major concern is that this infection, caused by T. indotineae, may be spreading internationally, and carrying antifungal resistance, it could pose a serious global public health problem. This review discusses five main aspects of T. indotineae: taxonomic classification, epidemiology, mechanism of drug resistance, diagnostic limitations, and management challenges leading to treatment failure. The mechanism of action of terbinafine is to bind and block the fungal enzyme squalene epoxidase, which is required to produce ergosterol, a component of the cell membrane. In resistant strains, point mutations occur in the squalene epoxidase gene, particularly Leu393Phe and Phe397Leu, changing the structure of the enzyme, and terbinafine cannot bind effectively, leading to treatment failure and recurrence. Resistance to alternative drugs like itraconazole and other azoles is also increasing through the overexpression of efflux pumps. In addition, several clinical and public health problems, such as the increasing use of over-the-counter corticosteroid creams, species identification delays, household transmission, and limited public health surveillance, have also contributed to the spread and resistance of this fungal infection. There are several knowledge gaps. Addressing this threat by T. indotineae requires standardised laboratories with genetic testing to identify the species; treatment guided by susceptibility; antifungal stewardship that selects the appropriate antifungal drug, dose, and treatment duration; regulation of the use of combination drugs; international surveillance; and high-quality, multicentre RCTs to establish evidence-based dosing regimens.

Keywords

Introduction

Dermatophytosis is the most prevalent superficial fungal infection and represents a significant public health concern (1–3). The World Health Organization (WHO) reported that dermatophyte infections affect approximately 25% of the global population (2, 4, 5). Dermatophytes affect the keratinous tissues, such as skin, hair, and nails, and clinically manifest as tinea corporis, tinea cruris, tinea pedis, tinea faciei, tinea barbae, tinea manuum, and tinea unguium, depending on the anatomical site. They are ecologically classified as geophilic (soil), zoophilic (animals), or anthropophilic (humans) (6–9). Emmons (1934) initially grouped them into three genera—Trichophyton, Microsporum, and Epidermophyton—whereas the current taxonomy includes seven genera, namely, Arthroderma, Trichophyton, Epidermophyton, Nannizzia, Paraphyton, Microsporum, and Lophophyton (10).

Conventionally, the allylamine antifungal agent terbinafine has been the first-line treatment for dermatophytosis (11, 12). Studies have reported an unprecedented surge of treatment failure cases due to resistant strains (13, 14). Indian dermatologists have reported the emergence of widespread, chronic, and antifungal-resistant dermatophytosis since around 2016 (15–17). Following 2016, isolates demonstrated higher minimum inhibitory concentrations (MICs) to terbinafine and atypical clinical presentations, accompanied by a surge in treatment failure cases (18–20). Based on these features and supported by molecular analysis, Kano et al. proposed the name Trichophyton indotineae in 2020 to distinguish these strains as a distinct species (21) Initially identified as Trichophyton mentagrophytes internal transcribed spacer (ITS) genotype VIII (22), it was later recognised as a separate species through comprehensive genetic analyses, including multilocus sequence typing and sequencing of the ITS region, which confirmed its unique genetic profile (23–25). Since the identification of T. indotineae (formerly part of the T. mentagrophytes/interdigitale complex), earlier reports primarily confined its presence to India and other Asian countries (26). Currently, the unprecedented global spread of T. indotineae poses a public health concern, potentially due to international travel (27). Therefore, the present review objective is to highlight the taxonomic reclassification, epidemiology, resistance mechanisms, and treatment challenges associated with T. indotineae, with the goal of contributing to improved patient management and control strategies. Combining the past and present knowledge by using a comprehensive search the present review aims to provide up-to-date knowledge to clinicians, clinical microbiologists, researchers, and public health practitioners to facilitate early and proper diagnosis for patient betterment, support antifungal stewardship, and strengthen strategies for the prevention and control of this emerging drug-resistant dermatophyte.

Taxonomic classification and identification

The morphological similarities between Trichophyton interdigitale and T. mentagrophytes within the T. mentagrophytes complex contribute to taxonomic challenges (24). Until 2007, T. mentagrophytes was described as a single morphological species, including T. mentagrophytes as zoophilic and T. interdigitale as anthropophilic variant (28). De Hoog et al. (2017) classified dermatophytes into seven clades using multilocus phylogeny, associating geophilic species with Arthroderma and anthropophilic ones with Epidermophyton and Trichophyton (29). T. indotineae (formerly T. mentagrophytes complex) was later found to be a complex of anthropophilic and zoophilic species, further blurring species boundaries (24–26). Studies from India in 2018 identified T. interdigitale as the primary dermatophyte, confirmed via ITS sequencing (18, 19). However, Nenoff et al. reclassified these isolates as T. mentagrophytes ITS genotype VIII (zoophilic), sparking debate (22). Choudhary et al. countered, suggesting an anthropophilic nature based on ITS and beta tubulin (BT) sequences (30). Subsequent multicentric studies found T. mentagrophytes ITS genotype VIII isolates exhibiting anthrophilic behaviour, possibly due to anthropisation and steroid misuse (31). Pchelin et al. and Singh et al. highlighted genomic overlap within the T. mentagrophytes/T. interdigitale complex (23, 32). Kano et al. reclassified T. mentagrophytes ITS genotype VIII as the new species T. indotineae (21). Later, Tang et al. confirmed the genotype’s clear genetic separation while noting its phenotypic similarity, suggesting that the new name is justified mainly on genetic rather than practical grounds (26). Nowadays, T. indotineae is considered a distinct species, based on molecular taxonomy. Thus, accurate taxonomic classification helps us understand the current epidemiological patterns of aetiology, evolutionary dynamics, and antifungal resistance associated with the emerging pathogen. As T. indotineae continues to spread globally and exhibits high rates of terbinafine resistance, harmonised taxonomic frameworks and standardised molecular diagnostic methods will be critical for surveillance and the development of evidence-based clinical and public health strategies.

Epidemiology of T. indotineae

Indian scenario

The atypical clinical presentation of dermatophytosis and chronic and recurrent cases were reported by Indian dermatologists (17, 33). Several studies highlight that the strains, T. indotineae (formerly T. mentagrophytes ITS genotype VIII), are responsible for this ongoing epidemic in India (20, 24, 25, 27). The presence of T. indotineae in India dates back more than a decade before the first articles on the topic were published, as evidenced by the earliest sequence submitted to GenBank (34). This sequence corresponds to a T. mentagrophytes ITS type VIII isolate, highlighting the long-standing but previously unrecognised presence of the isolates in the region. In 2014, Bhatia et al. reported the epidemiological shift from T. rubrum to T. mentagrophytes complex in an Indian scenario (35). A wide variation in the prevalence is mainly observed in North India, from 6.8% to as high as 61.5%, whereas from South India, it is 6.09% to 27.6% (36–38). Despite the hot and humid conditions in South India, a higher prevalence of dermatophytosis was reported in North India. Thus, Verma et al. suggested that this increased prevalence of dermatophytosis over 5–7 years was irrespective of climatic conditions (39). Dogra et al. reported from North India that over the past 3 to 4 years, there has been an alarming increase in dermatophytosis cases (15). These cases account for approximately 5–10% of newly registered patients in the dermatology outpatient departments in northern India (15). This suggests that hospitals encountering an epidemic like this alarming condition represent just the tip of the iceberg in the community. Between 2017 and 2019, T. indotineae emerged as the predominant dermatophyte species across India accounting for approximately 82.6% to 94% of isolates (40). In 2019 Nenoff et al. conducted a multicentric study covering the entire India and documented the upsurge of T. mentagrophytes/interdigitale complex 93.2% as a significant cause of dermatophytosis followed by T. rubrum (6.8%) (31).

This changing shift in the epidemiological pattern of causative agents may be due to multiple factors such as environmental factors (including temperature shift, humidity, and trauma), host factor (host susceptibility, host-parasite interaction), organism (changes in virulence patterns) (39). The increasing prevalence of T. indotineae infections, particularly those resistant to terbinafine, is largely attributed to the widespread misuse of over-the-counter fixed-dose topical combinations of antifungals, antibiotics, and potent corticosteroids such as clobetasol (11, 15, 41, 42). Studies show that 60–70% of tinea patients had prior exposure to such treatments (18, 39). Other contributing factors include poor hygiene, overcrowding, hot and humid working conditions, and tight-fitting synthetic clothing (39). Comorbidities such as diabetes and immunosuppression appear to play a minor role (43). Intra-familial transmission is frequent, with approximately 50% of patients reporting spread within the household, often linked to the sharing of contaminated personal items (34, 44, 45). Chronic dermatophytosis is a major public health concern and impairs quality of life, leading to prolonged treatment, frequent healthcare visits, reduced work productivity, and increased out-of-pocket expenditures. The widespread prevalence of T. indotineae has further amplified the clinical and socioeconomic burden of this disease. These factors collectively contribute to the rising burden and resistance seen with T. indotineae.

Global spread outside India

While T. indotineae was first recognised and widely reported in India, its presence has increasingly been documented across several countries, indicating a broader epidemiological footprint. Notably, Iran is another endemic region, with multiple studies confirming ITS sequences identical to T. indotineae, and the earliest documented cases dating back to 2008–2010 (46). A multicentre Iranian study (2016–2018) found that 28 out of 141 dermatophyte isolates within the T. mentagrophytes complex were T. indotineae, with a subset exhibiting high terbinafine MICs (≥32 mg/L), indicating antifungal resistance (34). In a 2019 survey conducted in Baghdad, 69.2% of T. mentagrophytes complex isolates were identified as T. indotineae, with terbinafine resistance detected in 39% of them (34). Overall, these findings suggest a potentially endemic presence of the pathogen in the region. Beyond the Indian subcontinent and the Middle East, imported cases of T. Indotineae have been increasingly reported across Europe, North America, and parts of Asia. Countries such as Belgium, Canada, Denmark, France, Germany, Greece, Japan, and Switzerland have documented confirmed cases, while Poland has deposited ITS sequences with 100% identity to T. indotineae in GenBank (21, 47–54). Although most of these cases were diagnosed post-2019, retrospective ITS sequencing revealed earlier instances—for example, a case as early as 2011 in Germany (55). Most patients were migrants from South Asian countries such as India, Pakistan, Bangladesh, Nepal, Sri Lanka, and Myanmar, suggesting that the entire Indian subcontinent may share a similar epidemiological profile (34). Additional cases were reported in individuals from Bahrain, Iraq, Libya, Saudi Arabia, Syria, Thailand, and Yemen, with isolated reports from Oman, Cambodia, Vietnam, and Australia (53–57). Figure 1 shows the timeline of key events in the emergence and global spread of T. indotineae. As a result, these reports suggest that the endemic range of T. indotineae may extend from the Middle East to Southeast Asia. In countries where the species is not considered endemic, local transmission cannot be ruled out. In Canada, for instance, one study reported an average delay of more than one year between patients’ migration from India and the onset of skin lesions, raising questions about local sources of infection. Refugee or migrant camps, where overcrowding and poor hygiene are common, may serve as hotspots for transmission in non-endemic regions (48). Global epidemiology of T. indotineae is shown in Figure 2, and Table 1.

Timeline illustrating the emergence and global dissemination of *Trichophyton indotineae* from 2008 to the present, highlighting major epidemiological, taxonomic, and clinical milestones, including the recognition of terbinafine resistance and expansion of global surveillance.
Figure 1. Timeline illustrating the emergence and global dissemination of Trichophyton indotineae from 2008 to the present, highlighting major epidemiological, taxonomic, and clinical milestones, including the recognition of terbinafine resistance and expansion of global surveillance.
Global epidemiology of *Trichophyton indotineae*: Countries are classified as endemic, imported cases, suspected local transmission, or no reported data, illustrating the expanding global spread of this emerging dermatophyte.
Figure 2. Global epidemiology of Trichophyton indotineae: Countries are classified as endemic, imported cases, suspected local transmission, or no reported data, illustrating the expanding global spread of this emerging dermatophyte.

Table 1. Geographic spread and resistance of T. indotineae.

Region/countryNotes on resistance
IndiaHigh prevalence (82–94% isolates); widespread terbinafine resistance
IranDocumented cases since 2008; terbinafine MIC ≥32 mg/L in resistant strains
Iraq (Baghdad)69.2% isolates identified as T. indotineae; 39% terbinafine resistance
Middle East (Saudi Arabia, Bahrain, Syria, Libya, Yemen)Multiple confirmed cases; resistance patterns emerging
Europe (Germany, France, Belgium, Denmark, Greece, Switzerland, Poland)Retrospective cases as early as 2011; migrants from South Asia primary source
North America (Canada, USA)Delayed onset post-migration suggests possible local transmission
Asia-Pacific (Japan, Thailand, Cambodia, Vietnam, Australia)Sporadic reports; surveillance limited

Although dermatophytosis may involve the scalp and hair, tinea capitis has not been established as a recognised clinical manifestation of T. indotineae. The clinical spectrum of T. indotineae is dominated by extensive tinea corporis and tinea cruris, with tinea faciei also frequently reported. In contrast, tinea manuum, tinea pedis, tinea barbae, and tinea unguium are less common (34). A 2025 systematic review of 64 patients found that infections predominantly involved multiple cutaneous sites, particularly the lower body and groin, and did not identify tinea capitis as an established clinical manifestation (58). Nevertheless, this apparent absence should be interpreted cautiously because T. indotineae is phenotypically difficult to distinguish from closely related members of the T. mentagrophytes complex. Prior scalp infections may therefore have been assigned to other taxa when molecular identification was not performed. Molecular surveillance of dermatophytes causing tinea capitis may help determine whether T. indotineae has an occasional role in scalp infection.

Risk factors and host susceptibility

There is a unique epidemiological pattern of T. indotineae infections that distinguishes these conditions from other forms of dermatophytosis. Statistical data show that both men and women are equally affected regardless of their age (59). Intrafamilial transmission is a hallmark of T. indotineae outbreaks, frequently spreading through close person-to-person contact, sexual transmission, or shared fomites such as clothing and towels (60). In non-endemic regions, a history of international travel to the Indian subcontinent—or close contact with individuals who have travelled from endemic areas—remains a major epidemiological link, though domestic, community-acquired transmission is increasingly reported globally (58).

Interestingly, T. indotineae primarily infects individuals with competent immunity. Though there may be certain co-morbid systemic conditions, such as diabetes mellitus and HIV infection, according to existing scientific evidence, they are not seen to be the risk factors for getting infected with this particular pathogen. Instead, it is the skin milieu and drug resistance that determine the course of the illness (45, 61).

The key factor for severe T. indotineae infections is improper usage of drugs and antifungal drug resistance. Improper use of OTC fixed-dose combinations (FDC) containing potent topical corticosteroids (such as clobetasol propionate) greatly increases the risk of the disease. Steroids provide quick, temporary symptom relief; however, they weaken the local immune response and alter the lesion’s normal appearance, making diagnosis difficult (58).

Allylamine (terbinafine) resistance

Terbinafine resistance in T. indotineae was first recognised in clinical settings when patients with dermatophytosis failed to respond to appropriate oral antifungal therapy. Despite adequate treatment, infections persisted or worsened, raising concerns regarding the underlying cause (62). This clinical resistance was later confirmed through in vitro studies, which revealed either complete resistance or significantly reduced susceptibility of the T. indotineae isolates to terbinafine (20, 21, 63). Such resistance is particularly prevalent among T. indotineae strains isolated from India (14, 18, 20). The exact timeline of the genetic mutations responsible for resistance remains unclear. However, by 2018, the first formal reports from India had documented in vitro terbinafine resistance in T. indotineae isolates (18, 19). A multicentre study conducted in India found that up to 76% of T. indotineae isolates exhibited resistance to terbinafine in vitro. Interestingly, even T. rubrum, another common dermatophyte species, also demonstrated resistance in 57.1% of tested isolates, highlighting the growing concern regarding allylamine resistance beyond T. indotineae (64). This alarming rise in terbinafine resistance represents a significant shift in treatment outcomes, as a substantial number of patients no longer respond adequately to either topical or oral terbinafine therapy (65). Although treatment failure has been most frequently documented in India (14, 27, 61), it is now being increasingly observed in other countries worldwide (66). Cases of tinea cruris and tinea corporis caused by T. indotineae are now emerging in these regions, suggesting a global trend that may continue unless appropriate measures are implemented (27, 67–69).

One of the major challenges in managing T. indotineae-related infections is the accurate identification of the species. Traditional morphological methods often fail to distinguish it reliably from other members of the T. mentagrophytes/interdigitale complex. Consequently, molecular techniques are essential for precise species identification (24, 26). Additionally, assessing antifungal susceptibility is crucial in determining treatment strategies (14, 65, 70). Terbinafine resistance can be confirmed using simple breakpoint methods or more accurate standardised microdilution assays, such as those outlined by the European Committee on Antimicrobial Susceptibility Testing (EUCAST) in Definition 11.0 and the Clinical and Laboratory Standards Institute (CLSI) (71, 72). Beyond susceptibility testing, sequencing the squalene epoxidase (SQLE) gene has become a key tool in confirming terbinafine resistance (18–20, 65, 73). Mutations in this gene are known to reduce or abolish the enzyme’s binding affinity for terbinafine, thereby rendering the drug ineffective (18). Figure 3 shows proposed mechanisms underlying terbinafine resistance in T. indotineae. Identification of these mutations provides definitive evidence of resistance and helps guide clinicians toward alternative treatment options. The emergence of SQEL mutations and the development of resistance to antifungals are multifactorial. Among them, selection pressure is one of the most important factors. Antifungal selection pressure is mainly associated with repeated exposure to antifungals, leading to the development of resistance in isolates. Empirical treatment without susceptibility testing and the widespread use of corticosteroid-antifungal combinations may create conditions that favor the persistence and transmission of resistant strains. Other factors, such as transmission within households and the absence of antifungal stewardship and public health surveillance, may also have contributed to the emergence of resistant genotypes in India and their eventual detection in multiple parts of the world. Given the increasing resistance patterns and the global spread of T. indotineae, it is imperative to adopt a comprehensive approach that involves accurate species identification, antifungal susceptibility testing, and molecular analysis of resistance mechanisms. Tailoring treatment based on this information is critical for achieving successful outcomes. This includes selecting appropriate oral or topical antifungal agents, potentially from other drug classes, when terbinafine resistance is confirmed (74).

Schematic representation of the mechanisms of terbinafine resistance in *Trichophyton indotineae.* The figure illustrates the normal inhibitory action of terbinafine on squalene epoxidase, the effect of SQLE mutations on drug binding, and additional resistance mechanisms including SQLE overexpression and increased drug efflux.
Figure 3. Schematic representation of the mechanisms of terbinafine resistance in Trichophyton indotineae. The figure illustrates the normal inhibitory action of terbinafine on squalene epoxidase, the effect of SQLE mutations on drug binding, and additional resistance mechanisms including SQLE overexpression and increased drug efflux.

Azoles (fluconazole and itraconazole) resistance

In the early clinical studies, fluconazole has been considered effective in treating dermatophytosis (75). However, several in-vitro antifungal susceptibility studies reported higher MIC for fluconazole against the T. indotineae (formerly T. mentagrophytes complex) (18, 19). Therefore, these results may raise questions about the therapeutic choice of fluconazole and underscore the need for additional clinical trials to assess its therapeutic reliability. Besides fluconazole, itraconazole has emerged as the most effective azole against dermatophytes (14). In vitro studies show that resistance to itraconazole is relatively rare (62, 76). Clinical data and antifungal susceptibility studies from northern India consistently identify itraconazole as an effective drug for better management of dermatophytosis compared to other azoles and the allylamine agent terbinafine (14). These findings support its continued use as a preferred treatment option for dermatophytosis in regions experiencing resistance to other antifungal agents.

Topical azoles also play a critical role in dermatophytosis management. Newer agents such as sertaconazole, luliconazole, lanoconazole, and efinaconazole demonstrate strong antifungal efficacy due to their low MIC values (20, 77). These topical treatments offer effective alternatives, particularly in mild or localised infections, and may reduce reliance on systemic therapy (77). Nevertheless, the potential for azole resistance remains a growing concern. Repeated or prolonged exposure to azoles was believed to contribute to the development of resistance (78). Studies have reported variable rates of azole resistance: a Mexican hospital using the E-test method found 19% fluconazole resistance among dermatophyte isolates (79), while an Indian study observed 35.4% fluconazole resistance in Trichophyton spp (18). The primary mechanism of azole resistance in dermatophytes involves the overexpression of efflux pump genes. These pumps actively expel antifungal drugs from fungal cells, reducing intracellular drug concentrations and limiting therapeutic effectiveness (80). Cervelatti and Fachin et al. first identified the MDR1 and MDR2 genes in T. rubrum (81). Further genomic analyses, such as those by Monod et al., identified 39 ATP-binding cassette (ABC) transporters and 170 major facilitator superfamily (MFS) transporters in the T. rubrum genome (82). Among these, only a subset of transporters recognised as functionally associated with azole resistance: four ABC transporters (TruMDR1, TruMDR2, TruMDR3, and TruMDR5) and two MFS transporters (TruMFS1 and TruMFS2). Exposure to azoles like itraconazole and voriconazole causes the overexpression of TruMDR1, TruMDR2, TruMDR3, and TruMFS2, confirming their role in resistance (82). Thus, itraconazole remains a potent systemic antifungal and several topical azoles are effective, azole resistance—driven by efflux pump overexpression—is an emerging threat. Ongoing surveillance and molecular studies are vital to guide treatment decisions and combat antifungal resistance in dermatophytes.

MIC distributions of the major antifungal agents tested against T. indotineae demonstrate considerable variability across isolates and studies. For terbinafine, both CLSI- and EUCAST-based studies consistently reported elevated MICs, with in vitro resistance observed in 78.9%–82.5% of isolates. MICs ≥4 μg/mL were reported in 70.5% of isolates tested by CLSI and 58.5% by EUCAST, consistent with the high prevalence of terbinafine resistance in T. indotineae. Elevated MICs have also been reported for griseofulvin and fluconazole, although standardised ECOFFs/ECVs or clinical breakpoints are not currently available for these agents.

For itraconazole, among 165 isolates evaluated using the CLSI methodology, 37.6% exhibited MICs ≥0.25 μg/mL, indicating a substantial proportion of isolates with elevated MICs. Voriconazole showed greater variability in susceptibility patterns, partly owing to differences in the proposed epidemiological cut-off values (0.125 versus 1 μg/mL). For posaconazole, CLSI data from 116 isolates revealed a bimodal MIC distribution, with approximately half of the isolates showing MICs ≤0.125 μg/mL and the remaining isolates predominantly exhibiting MICs of 0.125–0.5 μg/mL. Collectively, these findings indicate considerable heterogeneity in antifungal susceptibility among T. indotineae isolates and suggest the emergence of subpopulations with distinct MIC profiles (45).

Techniques for identification of Trichophyton indotineae

T. indotineae is closely related to T. mentagrophytes/interdigitale and cannot be reliably distinguished by conventional phenotypic methods. ITS sequencing is an important molecular approach that involves DNA extraction, PCR amplification, sequencing, and comparison with curated reference databases. Due to similarities among related species, e.g., the T. mentagrophytes/interdigitale complex, and the limitations of existing databases, misidentification may occur; therefore, regularly updated databases and well-characterised reference strains are essential. Specific nucleotide differences in the ITS region can aid identification. Thus, ITS sequencing is reliable, although it requires multiple processing steps, including access to sequencing facilities, and a relatively long turnaround time, which limits its routine use. Alternative approaches include species-specific PCR, PCR-RFLP, and quantitative PCR (qPCR). PCR-RFLP targeting TOP2 and species-specific PCR targeting the C120–287 locus have demonstrated high specificity (83, 84). qPCR assays targeting T. indotineae-specific ITS polymorphisms facilitate the rapid detection of T. indotineae directly from clinical specimens; however, further optimisation and validation are required to ensure high specificity (85). Apart from the molecular tool, the proteomic method using an improved MSI-2 MALDI-TOF database enabled rapid and accurate identification of T. indotineae. Therefore, the incorporation of reference spectra increases identification from 5% to 96%, with a sensitivity of 99.6% for the identification of T. indotineae (86).

Treatment and management challenges

Therapeutic failure

Therapeutic failures in T. indotineae infections are increasingly reported due to high-level resistance to terbinafine, traditionally the first-line agent for dermatophytosis. The primary mechanism involves point mutations in the squalene epoxidase (SQLE) gene, particularly Leu393Phe and Phe397Leu, which reduce drug binding and render terbinafine ineffective (30, 87). Apart from these common mutations, other point mutations were also documented, including L393S, F397I, F397V, F415I, F415S, F415V, H440Y, I121M/V237I, S395P, Q408L, and S443P in the squalene epoxidase gene. As a result, empirical treatment without prior susceptibility testing is often inadequate and contributes to treatment failure, prolonged morbidity, and further transmission. In India and other affected regions, high recurrence rates and chronicity of infection are now linked to the widespread circulation of these resistant genotypes (65).

Alternative therapies

Itraconazole has emerged as the most widely used systemic alternative in areses of terbinafine resistance. However, emerging reports indicate reduced susceptibility or resistance to azoles as well, likely due to overexpression of efflux pumps and mutations affecting ergosterol biosynthesis (88). Based on recent evidence and expert recommendations, terbinafine 250 mg twice daily is the preferred choice, mainly because of higher terbinafine MICs, given the high prevalence of squalene epoxidase mutations in the ERG1 gene. Meanwhile, itraconazole 100 mg/day remains an effective first-line option, and it doesn’t offer a clear benefit over 200 mg/day in terms of cure rates. Therapy should be individualised and continued until complete clinical and mycological cure, with close surveillance for relapse and implementation of antifungal stewardship by selecting the appropriate antifungal, dose, and treatment duration (62). Other newer triazoles, such as voriconazole and luliconazole, have shown promise in vitro, but their clinical efficacy in recalcitrant T. indotineae infections remains underexplored (19). Topical monotherapy, particularly with over-the-counter combinations containing corticosteroids, is ineffective for widespread or resistant infections and may exacerbate disease by suppressing local immunity (70). Clinical diagnostic and management algorithm for T. indotineae is shown in Figure 4.

Clinical diagnostic and management algorithm for *Trichophyton indotineae*: The algorithm outlines the sequential approach from clinical suspicion and laboratory diagnosis to species confirmation, antifungal susceptibility testing, treatment selection based on terbinafine susceptibility, and follow-up with preventive measures.
Figure 4. Clinical diagnostic and management algorithm for Trichophyton indotineae: The algorithm outlines the sequential approach from clinical suspicion and laboratory diagnosis to species confirmation, antifungal susceptibility testing, treatment selection based on terbinafine susceptibility, and follow-up with preventive measures.

Need for antifungal stewardship

The irrational and unregulated use of combination creams—often containing potent corticosteroids with antifungals and antibacterials—is a major contributor to resistance and therapeutic failure in India and similar settings (70). Antifungal stewardship must prioritise proper diagnosis, culture and susceptibility testing, and patient counselling. Tailored treatment protocols and national guidelines should discourage empirical combination therapy and promote evidence-based regimens. Public education on avoiding self-medication and completing treatment courses is equally crucial.

Public health implication

The transcontinental spread of T. indotineae illustrates global gaps in dermatophyte surveillance, antifungal resistance monitoring, and public health policy. Unlike bacterial infections, fungal resistance data is rarely integrated into national surveillance systems, hindering coordinated response efforts. Moreover, limited access to molecular diagnostics in many regions delays accurate identification and appropriate treatment. Regulatory oversight of antifungal and corticosteroid combinations in over-the-counter products is inadequate, especially in developing countries, facilitating misuse. A concerted global effort involving clinicians, microbiologists, policymakers, and pharmaceutical stakeholders is needed to address the spread of resistant dermatophytes and mitigate future outbreaks (27).

Recommendations

To effectively combat the emergence and spread of T. indotineae, several coordinated strategies must be implemented. To implement this, there is a need for a WHO-coordinated fungal priority pathogen surveillance framework, complemented by existing antifungal resistance surveillance initiatives such as SENTRY and EUCAST/CESAR, which should be adapted to establish dermatophyte-specific surveillance to monitor species distribution, antifungal susceptibility, and resistance trends. Firstly, in a resource-limited laboratory setting, direct KOH microscopy, fungal culture, and terbinafine resistance screening using targeted PCR-based assays should be effective diagnostic approaches. At the same time, MALDI-TOF MS and sequencing should be strengthened in regional reference laboratories. Standardised antifungal stewardship programs should promote rational prescribing, optimise dosing and treatment duration, and discourage inappropriate use of topical corticosteroid–antifungal combinations. Finally, there is a critical research gap due to the absence of adequately powered randomised controlled trials (RCTs) evaluating treatment strategies specifically for T. indotineae. Thus, there is a need to develop high-quality multicentre RCTs to establish evidence-based dosing regimens, treatment duration, combination therapy, and the role of newer antifungal agents in the management of recalcitrant dermatophytosis.

Conclusion

The rapid rise in T. indotineae infections, which cause widespread dermatophytosis across India, neighbouring countries, and Europe, has become a significant public health concern. Terbinafine resistance complicates treatment, though itraconazole remains the preferred option despite emerging azole resistance. Clinicians should suspect T. indotineae in widespread infections, especially in patients from endemic regions. Molecular diagnostic capabilities remain limited, thus highlighting the need for routine testing of in vitro antifungal susceptibility, particularly for terbinafine and itraconazole. Urgent measures include banning over-the-counter sales of antifungal-steroid combinations, ensuring prescription-only drug use, and engaging policymakers to enforce regulations. Accurate species identification and antifungal susceptibility testing are essential for better therapeutic management of the increasingly prevalent and drug-resistant pathogen.

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Footnotes

Edited by: Esperanza Duarte-Escalante, National Autonomous University of Mexico, Mexico

Reviewed by: Sunna Nabeela, Lundquist Institute for Biomedical Innovation, United States

María Del Rocío Alicia Reyes-Montes, National Autonomous University of Mexico, Mexico

Patricia Manzano-Gayosso, National Autonomous University of Mexico, Mexico

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Conflict of interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Funding

The author(s) declared that financial support was received for this work and/or its publication. Funding was received from American University of Antigua College of Medicine for the publication of this article.

Author contributions

DS: Conceptualization, Data curation, Writing – original draft. AO: Writing – review & editing. MS: Writing – review & editing. MC: Writing – review & editing, Supervision. CB: Writing – review & editing, Supervision. NM: Writing – review & editing, Supervision. DB: Software, Writing – review & editing. SR: Writing – review & editing. PH: Writing – review & editing, Conceptualization, Funding acquisition, Supervision.

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Citation

Shaw, D., et al. (2026). The global emergence of Trichophyton indotineae: epidemiology, resistance, and management challenges. Frontiers in Tropical Diseases, Volume 7. https://doi.org/
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Copyright © 2026 Shaw, Omar, Singh, Chandanathil, Bhargavi, Mysore, Bir, Ramasamy and Honnavar.

License: https://creativecommons.org/licenses/by/4.0/

*Correspondence: Prasanna Honnavar

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